ε-聚赖氨酸对金黄色葡萄球菌生长及生物膜形成的影响#br#

目的 研究ε-聚赖氨酸(ε-poly-L-lysine, ε-PL)对金黄色葡萄球菌(Staphylococcus aureus, S. aureus)生长及生物膜形成的影响。方法 以金黄色葡萄球菌标准菌株ATCC25923及社区获得性耐甲氧西林金黄色葡萄球菌(methicillin-resistant Staphylococcus aureus, MRSA)USA300为试验菌株,常量肉汤稀释法(试管)测定最低抑菌浓度(minimum inhibitory concentration, MIC),酶标仪检测吸光度法观察各株金黄色葡萄球菌的生长曲线,96孔板结晶紫染色法检测各株菌生物膜的形成并用扫描电子显微镜(SEM)观察生物膜的形成情况。结果 ε-PL对ATCC25923和USA300的MIC均为31.25mg/mL。ε-PL浓度升高时对两株菌生长的抑制作用随之增强。1/2MIC ε-PL能显著降低ATCC25923和USA300生物膜的形成能力。 结论 ε-PL作为一种安全、高效的天然防腐剂,能有效抑制金黄色葡萄球菌细菌的生长及生物膜的形成,为新型药物的研发提供了理论依据。     

耐甲氧西林金黄色葡萄球菌医院感染危险因素及耐药性分析

<正>金黄色葡萄球菌是引起医院感染的重要病原菌之一,随着广谱抗生素的广泛使用,耐甲氧西林金黄色葡萄球菌(Methicilin-resistant Staphylococcus aureus,MRSA)的发生率逐渐上升,成为医院感染控制的难点。患者一旦发生MRSA医院感染,增加病痛,延长住院时间,增加医疗费用,将严重威胁患者的健康和生命。有效监测MRSA感染病例,对预防和控制MRSA医院感染的发生、确保医疗质量和医疗安全有重要     

耐甲氧西林金黄色葡萄球菌确证及药物敏感试验方法学比较

<正>葡萄球菌是人类感染的最重要的病原菌之一,其中耐甲氧西林金黄色葡萄球菌(methicillin resistant staphylococcus aureus,MRSA)所造成的院内感染日趋严重,由MRSA引起的感染已经成为临床抗感染治疗的难题之一。金黄色葡萄球菌为临床常见病原菌,能产生多种毒素、酶及抗原蛋白,具有较强的致病性,能引起皮肤软组织感染、血流感染及全身各脏器感染。1961年临床首次分离出MRSA,该菌对所有β-内酰     

金黄色葡萄球菌的检测分析

目的通过调查金黄色葡萄球菌(Staphyloccocus aureus Rosenbach)医院感染的危险因素的分析,总结采用纸片扩散法为选择合理药物治疗提供科学依据临床。方法回顾性分析,2002年1月至2010年1月我院诊治的435例金黄色葡萄球菌患者的临床资料,临床采用纸片扩散法进行药敏试验。结果 8年来从各类临床标本中分离出435株金黄色葡萄球菌,其中包括170株耐甲基西林金黄色葡萄球菌。金黄色葡萄球菌对万霉素、利福平、头孢哌酮、丁胺卡那素、头孢唑林、庆大霉素、环丙沙星、青霉素G的敏感率分别为99.5%、97.8%、77.8%、77.8%、70.1%、59.7%、2.1%。结论随着耐甲基西林金黄色葡萄球菌感染趋势的不断上升,用纸片扩散法进行药敏试验更具有临床优势,可以更好的选择药物合理治疗。     

MecI基因缺失在耐甲氧西林金黄色葡萄球菌中的检测情况

<正>金黄色葡萄球菌(staphylococcus aureus)是人类一种重要的病原菌,可引起局部化脓感染,也可引起肺炎、伪膜性肠炎、心包炎,甚至败血症、脓毒症等全身感染。但随着耐甲氧西林金黄色葡萄球菌(MRSA)的不断出现,金黄色葡萄球菌引起感染的治疗成为临床一个重大的难题。MRSA主要的耐药机制是因为获得了外源性的耐药基因Mec A。Mec A基因的表达受多种因素的影响,其中Mec I基因为负性调节因子,其     

耐甲氧西林金黄色葡萄球菌感染的研究进展

凡对甲氧西林、苯唑西林耐药或Mec基因阳性的金黄色葡萄球菌定义为耐甲氧西林金黄色葡萄球菌(methicillin resistant staphylococcus aureus MRSA),由于其致病力强,传播速度快,常出现多重耐药性,在院内播散可导致病区内的暴发流行,其耐药机制非常复杂,治疗难度大,病死率高,已成为医院感染中的严重问题。笔者就MRSA的感染现状、耐药机制及治疗进展综述如下。     

抗MRSA感染新药的应用与研究进展

抗耐甲氧西林金黄色葡萄球菌(methicillin-resistant Staphylococcus aureus,MRSA)感染和对多重耐药金黄色葡萄球菌的治疗一直是临床的严峻挑战.头孢洛林、达巴万星、特地唑胺和奥利万星是美国FDA最新批准的用于抗MRSA感染的药物,本文将对它们的结构特点与作用机制、体内外抗菌活性、不良反应以及临床应用与未来发展进行综述,并着重分析其特性和优劣势.     

355株金黄色葡萄球菌药敏试验结果分析

目的：探讨金黄色葡萄球菌（S-aureus）对抗菌药物的敏感性,为临床应用抗生素提供科学依据。方法：按《全国临床检验操作规程》对S—aureus进行培养分离鉴定,采用纸片扩散法进行药敏试验,参照美国国家临床实验室标准化委员会标准（NCCLS）读取结果。结果：8年来从各类临床标本中分离出355株S—aureus,其中耐甲氧西林金黄色葡萄球菌（MRSA）为140株。金黄色葡萄球菌对万古霉素、利福平、头孢哌酮、丁胺卡那霉素、头孢唑啉、庆大霉素、环丙沙星、氟哌酸、氨苄西林、青霉素G、苯唑西林的敏感率分别为100．0％、97．8％、76．1％、76．1％、69．9％、60．3％、60．1％、54．7％、3．9％、2．1％、0．9％。结论：MRSA感染呈上升趋势,青霉素类已不能成为治疗S—aureus感染的一线药物,万古霉素、利福平可作为治疗S—aureus感染的首选药物。     

苯唑西林敏感耐甲氧西林金黄色葡萄球菌(OS-MRSA)研究进展

摘要：金黄色葡萄球菌(Staphylococcus aureus, SA)是导致医院内感染及社区获得性感染的一种常见病原菌，可引起宿主 不同部位的感染，感染类型多样。耐甲氧西林金黄色葡萄球菌(methicillin resistant Staphylococcus aureus, MRSA)呈现对多种类 型抗菌药物的耐药特征，其在不同国家和地区的检出率和流行特征存在明显差异。随着对MRSA耐药性和耐药机制研究的不 断深入，一种具有特殊耐药特征的MRSA亚群逐渐被报道，即苯唑西林敏感的耐甲氧西林金黄色葡萄球菌(oxacillin-susceptible methicillin-resistant Staphylococcus aureus，OS-MRSA)。OS-MRSA典型特征为携带抗药性基因mecA，但其对苯唑西林的MIC值 较低(通常＜4mg/L)。由于目前临床实验室主要采用苯唑西林和或头孢西丁药敏试验方法来区分MRSA及甲氧西林敏感金黄色葡 萄球菌(MSSA)，而很少应用基因检测方法(mecA基因)进行检测或确认，因此OS-MRSA常被错误报告为MSSA，临床依据药敏 报告进行抗感染治疗，常导致治疗失败及患者病死率的增加。此外，OS-MRSA菌株在不同国家和地区人群分离率及其分子流 行病学特征存在较大差异。因此，本文将从分子流行病学、实验室检测方法、耐药机制、毒力特征及临床治疗等5个方面对OSMRSA 的最新研究进展进行综述。     

社区及院内耐甲氧西林金黄色葡萄球菌感染的临床特征比较及耐药性分析

<正>金黄色葡萄球菌(staphylococcus aureus,SAU)是院内感染常见的革兰染色阳性球菌,获得mec A基因或苯唑西林最低抑菌浓度(MIC)≥2μg/ml的菌株称为耐甲氧西林金黄色葡萄球菌(MRSA)[1]。本文对我院2014年1月至2016年3月住院期间检出MRSA的所有患者进行回顾性调查,对医疗机构相关MRSA(HA-MRSA)及社区MRSA(CA-MRSA)感染     

Recombinant human DNase I decreases biofilm and increases antimicrobial susceptibility in staphylococci

Extracellular DNA is an adhesive component of staphylococcal biofilms. The aim of this study was to evaluate the antibiofilm activity of recombinant human DNase I (rhDNase) against Staphylococcus aureus and Staphylococcus epidermidis. Using a 96-well microtiter plate crystal-violet binding assay, we found that biofilm formation by S. aureus was efficiently inhibited by rhDNase at 1-4?μg?l?1, and preformed S. aureus biofilms were efficiently detached in 2?min by rhDNase at 1?mg?l?1. Pretreatment of S. aureus biofilms for 10?min with 10?mg?l?1 rhDNase increased their sensitivity to biocide killing by 4-5 log units. rhDNase at 10?mg?l?1 significantly inhibited biofilm formation by S. epidermidis in medium supplemented with sub-MICs of antibiotics. We also found that rhDNase significantly increased the survival of S. aureus-infected Caenorhabditis elegans nematodes treated with tobramycin compared with nematodes treated with tobramycin alone. We concluded that rhDNase exhibits potent antibiofilm and antimicrobial-sensitizing activities against S. aureus and S. epidermidis at clinically achievable concentrations. rhDNase, either alone or in combination with antimicrobial agents, may have applications in treating or preventing staphylococcal biofilm-related infections.     

重组溶葡萄球菌酶对金黄色葡萄球菌生物被膜的体外清除作用

目的研究重组溶葡萄球菌酶对金黄色葡萄球菌生物被膜的体外清除作用。方法使用硅橡胶膜片建立金黄色葡萄球菌生物被膜的体外模型;使用超声震荡—活菌计数法作为金黄色葡萄球菌生物被膜的定量检测方法,分别测定在给予重组溶葡球菌酶及其对照药作用前后金黄色葡萄球菌生物被膜中的活菌数;使用扫描电镜作为金黄色葡萄球菌生物被膜的直观定性检测方法,分别观察在给予重组溶葡球菌酶及其对照药作用前后金黄色葡萄球菌生物被膜的镜下形态。结果经72 h连续培养,金黄色葡萄球菌在硅橡胶片上形成较为成熟的生物被膜,不同浓度重组溶葡球菌酶作用24 h后被膜中的活菌计数明显低于对照药去甲万古霉素,电镜结果进一步支持此结果。结论重组溶葡萄球菌酶能够有效地清除金黄色葡萄球菌生物被膜。     

Activity of daptomycin on biofilms produced on a plastic support by Staphylococcus spp

The aim of this study was to assess whether the novel lipopeptide daptomycin might be capable of disrupting or inhibiting the synthesis of biofilms produced by staphylococci. Fourteen recently isolated slime-producing methicillin-susceptible (MET-S) and methicillin-resistant (MET-R) strains (three MET-S Staphylococcus aureus, three MET-R S. aureus, three MET-S Staphylococcus epidermidis, three MET-R S. epidermidis and two vancomycin-intermediate S. aureus (VISA)) were tested. Slime formation on polystyrene plates was quantified spectrophotometrically. Daptomycin (2-64 mg/L) inhibited slime synthesis by > or =80% in MET-S strains, by 60-80% in MET-R S. aureus and by 70-95% in MET-R S. epidermidis. At 64 mg/L, biofilm synthesis decreased by 80% in the VISA isolates. Daptomycin also disrupted pre-formed biofilm: >50% breakdown of initial biofilm (5h) was observed in all strains. Disruption of mature biofilms (48 h), in terms of percentage, was more variable depending on the strain, ranging from ca. 20% in a MET-R S. epidermidis strain to almost 70% in two MET-S strains (one S. aureus and one S. epidermidis). Daptomycin at concentrations achievable during therapy promoted a statistically significant inhibition of slime synthesis (preventing biofilm building) and induced slime disruption (disaggregating its structure) both in initial and mature biofilms on a plastic support in all staphylococcal strains studied.     

药物协同抗生物膜研究进展

生物膜是细菌或真菌附着于物体表面所形成的有一定结构和功能的菌细胞群体, 其最显著的特征之一是高度耐药性, 单用一种抗菌药物很难将其完全清除, 而不同种类药物的联合应用可有效清除生物膜。本文 现就近年来针对铜绿假单胞菌、葡萄球菌、大肠杆菌、白念珠菌等常见病原菌生物膜的药物协同干预作用作一综述。     

Adenotonsillar disease

Adenotonsillar disease (adenoiditis and recurrent tonsillitis) is a prevalent otolaryngologic disorder aetiologically based on chronic inflammation triggered by a persistent bacterial infection. These bacteria, mostly Staphylococcus aureus, Haemophilus sp., and Streptococcus sp., persist predominantly intracellular and within mucosal biofilms. The recurrent or chronic inflammation of the adenoids and faucial tonsils leads to chronic activation of the cell-mediated and humoral immune response, resulting in hypertrophy of the lymphoid tonsillar tissue. This hypertrophic tissue is the cause for the prominent clinical symptoms: obstruction of the upper airways, snoring, and sleep apnea for adenoiditis or sore throat, dysphagia and halitosis for recurrent tonsillitis. Treatment strategies should target the persisting bacteria within their biofilm or intracellular shelter. Macrolide antibiotics like clarithromycin are able to modulate the immune system and to interfere in bacterial signaling within biofilms. Clindamycin, quinupristin-dalfopristin, and oritavancin are intracellular high active compounds. Surgical removal of the hypertrophic tissue by modern procedures like laser tonsil ablation, eliminates not only a mechanical obstacle of the airways, it removes also the basis for the aetiologic cause, the "biofilm carrier". This review summarizes the role of bacterial persistence in mucosal biofilms for the aetiology, diagnosis and treatment of adenotonsillar disease and relevant patents.     

Higher biofilm formation in multidrug-resistant clinical isolates of Staphylococcus aureus

The biofilm-forming capacity of Staphylococcus aureus contributes to antibiotic resistance, but whether antibiotic-resistant strains have the capacity to form biofilms has not yet been determined. Therefore, we recovered 101 clinical isolates of S. aureus and performed antibiotic susceptibility testing for 30 antibiotics using a VITEK II automatic system. We then carried out a biofilm assay on 96-well polystyrene plates. In addition, the presence of IS256 involved in the variation of biofilm phases of S. aureus was determined by polymerase chain reaction. The prevalence of IS256 was significantly related to multidrug resistance as well as biofilm expression, with biofilm positivity in 27 (39.7%) of the 68 IS256-positive strains and 3 (9.1%) of the 33 IS256-negative strains. In our analysis of the relationship between meticillin resistance and biofilm formation, we found that the rate of biofilm positivity was 37.9% (25/66) for meticillin-resistant strains and 14.3% (5/35) for meticillin-susceptible strains (P<0.05). Staphylococcal cassette chromosome mec (SCCmec) typing found that SCCmec type IV was most prevalent, comprising 14 (56.0%) of the 25 biofilm-positive, meticillin-resistant strains. A statistical analysis testing the relationship between multidrug resistance and biofilm formation revealed a significantly higher rate of biofilm development in strains with greater multiresistance compared with strains with less multiresistance. Our results suggest that the multidrug-resistant clinical isolates of S. aureus have a greater likelihood of developing biofilms on medical devices.     

单宁酸联合氟康唑抑制金黄色葡萄球菌与白念珠菌混合生物膜的作用及机制研究

摘要：目的 分析单宁酸联合氟康唑降低金黄色葡萄球菌与白念珠菌混合生物膜的作用及其机制。方法 收集2019年临床 分离的3株耐甲氧西林金黄色葡萄球菌(MRSA),分别命名为SA1,SA2和SA3;利用分光光度法检测单宁酸单独或联合氟康唑对 金黄色葡萄球菌与白念珠菌DAY185混合菌群生长能力的影响,进一步采用结晶紫染色法测定对混合生物膜形成能力的影响; 扫描电子显微镜观察单宁酸联合氟康唑对混合生物膜结构影响;实时荧光定量PCR(qRT-PCR)检测白念珠菌DAY185生物膜形成 相关基因(ALS1、ALS3和RBT1)和SA1生物膜形成相关基因(icaA、sarA和cidA)的表达量变化。结果 单宁酸可以降低金黄色葡萄 球菌与白念珠菌混合菌群的生长能力和混合生物膜形成能力,当联合氟康唑时抑制作用更加明显;扫描电子显微镜显示单宁酸 联合氟康唑可以明显减少金黄色葡萄球菌在白念珠菌菌丝上的黏附;qRT-PCR结果表明：单宁酸联合氟康唑主要可以降低混合 生物膜中白念珠菌ALS3基因(P＜0.05)和金黄色葡萄球菌icaA和sarA基因(P＜0.05)的表达量。结论 单宁酸联合氟康唑可以降低 金黄色葡萄球菌与白念珠菌混合生物膜的形成,其机制主要通过降低白念珠菌菌丝形成相关基因ALS3和金黄色葡萄球菌黏附相 关基因icaA和sarA的表达水平。     

Activity of moxifloxacin on biofilms produced in vitro by bacterial pathogens involved in acute exacerbations of chronic bronchitis

The aim of this study was to assess whether moxifloxacin is able to inhibit the synthesis of and to disrupt biofilms produced in vitro by bacterial pathogens involved in acute bacterial exacerbations of chronic bronchitis. Three strains each of Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Staphylococcus aureus and Escherichia coli recently isolated from clinical respiratory specimens and capable of slime production were used. Biofilm formation on polystyrene plates was quantified spectrophotometrically by established methodologies. Moxifloxacin (0.5 mg/L) inhibited slime synthesis by >70% in S. aureus, H. influenzae and S. pneumoniae, 45-70% in E. coli and 35-70% in M. catarrhalis. Disruption of pre-formed structures was also promoted by moxifloxacin both for initial (5h) and mature (48 h) biofilms. Drug concentrations reached during therapy (0.5-4 mg/L) resulted in a breakdown of initial biofilm of 60-80% in H. influenzae and S. pneumoniae, 48-86% in S. aureus, 37-69% in M. catarrhalis and 51-71% in E. coli. Mature biofilms were less susceptible to degradation. Moxifloxacin at concentrations that can be achieved in the bronchial mucosa during therapy therefore promotes a significant inhibition of biofilm synthesis and induces slime disruption, a feature that may be instrumental in reducing the exacerbations so frequently observed in this condition.     

Anti-Staphylococcal Biofilm Effects of Human Cathelicidin Peptides

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Use of an oxonol dye in combination with confocal laser scanning microscopy to monitor damage to Staphylococcus aureus cells during colonisation of silver-coated vascular grafts

The antimicrobial silver-coating of medical prostheses is regarded as a means to reduce the risk of bacterial colonisation after implantation. The effect of a silver-coating of vascular grafts on biofilm formation was assessed in batch cultures of Staphylococcus aureus, using confocal laser scanning microscopy. Total cells in biofilms were analysed by staining with the DNA-binding fluorochrome SYTO 62 and the proportion of damaged cells was quantified with the membrane potential-sensitive dye bis-(1,3-dibutylbarbituric acid) trimethine oxonol. Both the extent of biofilm formation and the proportion of viable biofilm cells were significantly diminished on the surface of the silver-coated vascular grafts compared with uncoated controls, probably due to the antimicrobial activity of silver ions released from the silver-coated graft surface.